Tag: Trigeminal neuralgia treatments

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FPA – New Life for Cancer Drug

  • Published October 11, 2021

New life for cancer drug that reprograms pain pathway to fight chronic pain

Chronic pain associated with nerve injury and chronic bone pain from metastatic cancer are unmet medical needs. This sober sentence vastly understates the crushing and devastating impact of these forms of pain on victims’ lives, their families, and their social and professional lives.

“I just can not sleep any more because turning in bed hurts, my spine hurts lying down, and sitting up to sleep hurts even more. During daytime, I have constant brain fog, interrupted by pain that within minutes gets worse (10-out-of-10) against a background of constant burning pain which gets worse toward the afternoon and evening. I hurt more when I go to the bathroom. The pain medication makes my brain fog worse, I feel like a zombie, I am badly constipated and itch all over.” That is how a patient with bone cancer pain feels. Testimony from victims of chronic nerve injury pain, through peripheral nerve damage from diabetes or medications, or in the aftermath of shingles, indicates that their lives are equally turned upside down from the pain.

New treatments against pain are needed. What is the desired profile ? “New drugs and other therapies against chronic pain need to be safe, i.e the fewer side effects the better, especially non-addictive and non-sedative, and effective. For example they should work against nerve injury pain and cancer pain, finally and practically, with minimal time to official drug approval. “Since chronic pain, like many chronic diseases, has an important root in genetic switches being reprogrammed in a ‘bad’ way, a disease-modifying treatment for chronic pain should reset the genetic switches, not just cover up the pain as with opioid and aspirin/tylenol-like painkillers,” says Dr. Wolfgang Liedtke, who practiced pain medicine for the last 17 years at Duke University Medical Center in Durham, NC, USA, and directed the former Liedtke-Lab to elucidate basic pain mechanisms. Dr. Liedkte moved to an executive position at Regeneron Pharmaceuticals in Tarrytown NY, in April 2021.

Liedtke’s Duke team, jointly with colleagues from University of California Irvine, tackled the problem by starting with a collection of “junkyard of cancer drugs”, 1,057 compounds originating from two Compound Libraries of the National Cancer Institute. Liedtke picked cancer drugs because a sizeable number of them influence epigenetic regulation of genes, which stops rapidly dividing cancer cells from dividing, but can reset maladaptive genetic switches in non-dividing nerve cells. In order to identify useful candidate anti-pain drugs from this starting pool, Liedtke’s team devised a screening method that relied on brain nerve cells from genetically-engineered mice that were “knockin” for a convenient reporter gene system so that compounds that enhance expression of an anti-pain target gene would generate a bio-luminescent signal which can be readily measured, allowing 1,057 compounds to be tested.

The selected anti-pain target gene was Kcc2 which encodes a chloride extruding transporter molecule, KCC2. KCC2 churns out chloride from nerve cells, low chloride means strong function of inhibitory neurotransmission, also in pain pathways, thus silencing the pain signal, or not allowing it to break through. In essentially all forms of chronic pain studied in experimental animals and also human spinal cord models, KCC2 disappears from the primary pain gate in the dorsal spinal cord. Liedtke’s team identified 137 first-round winners, i.e Kcc2 gene expression-enhancers, which then were retested iteratively, with a yield of four final co-winners. Kenpaullone was selected for work-up because the compound had a strong record of protecting nerve cells in human ALS models, also hearing and brain neurons from damage. In mice, Kenpaullone functioned effectively against pain caused by nerve constriction injury and by cancer cells seeding in the femur. Pain relief was profound, long lasting and with protracted onset, indicative of Kenpaullone impacting gene regulation.

Says Liedtke “At this stage, we knew we had met the basic requirement of our screen of shelved cancer drugs, namely identified Kcc2 gene expression-enhancers, and demonstrated that they are analgesics in valid preclinical pain models.” Thus encouraged, Liedtke’s team addressed whether Kenpaullone affected spinal cord processing of pain, with affirmative findings, then whether the pain-relaying nerve cells in the dorsal spinal cord can lower their elevated chloride, caused by nerve injury, by Kenpaullone treatment – again with resoundingly affirmative results. This was great news and prompted the investigators to query how exactly Kenpaullone works in nerve cells so that the Kcc2 gene is expressed stronger.

They discovered the underlying signaling mechanism, a key element of it completely new. Kenpaullone inhibits the kinase GSK3-beta which adds phosphate tags to other proteins which in turn switches their function powerfully. They found that the kinase target of GSK3beta is delta-catenin, delta-cat, which when phosphorylated is tagged for the cellular garbage bin. That means that chronic pain, via activation of GSK3-beta leads to loss of delta-cat in pain relaying neurons. What is the original function of delta-cat in relation to pain relay, and in relation to gene expression of Kcc2 ?  Liedtke’s team found that non-phosphorylated delta-cat transfers into the cell’s nucleus and binds to the Kcc2 gene’s DNA in its promoter region, where it switches back on the switched-off Kcc2 gene. To prove the relevance of this pathway for pain, they devised a gene-therapeutic approach so that phosphorylation-resistant delta-cat becomes the payload of an AAV9 gene-therapy viral vector, which infects spinal cord dorsal horn neurons. Injection of this gene therapy vector into the cerebrospinal fluid of mice was similarly analgesic as Kenpaullone.

These findings suggest that Kenpaullone and similarly-acting kinase-inhibitory compounds, also delta-cat gene therapy can become new tools in our toolbox against chronic “refractory” pain, also caused by nerve injury, also caused by cancer bone pain, likely against other forms of chronic pain where Kcc2 is not expressed well (trigeminal pain), and possibly other neurologic and psychiatric disorders where this mechanism appears to contribute to disease.

Amidst Duke co-authors, 1st author Dr. Michele Yeo successfully elucidated basic regulation of the Kcc2 gene together with Liedtke for more than a decade and ran the 1,057 compound screen, co-first author Dr. Yong Chen provided skillful animal experimentation, and co-senior author Dr. Ru-Rong Ji (Director of Translational Pain Research) and his team covered dedicated assessment of spinal cord relay mechanisms. Collaboration with Dr Jorge Busciglio’s laboratory at UC Irvine was key to validate human relevance of Kenpaullone.

Summary Figure
Upper right “Junkyard of cancer” drugs were screened, akin to sieving through sand, looking for gold nuggets. Kenpaullone was identified as a “winner”, capable of switching on the Kcc2 gene, which previous research predicted to be beneficial for chronic pain.
Upper left Nerve injury pain and bone cancer pain are serious and pressing unmet medical needs. Preclinical models were used totest Kenpaullone which proved to be highly effective in both.
Middle panels, left-hand Nerve injury by constriction or cancer cells populating a bone activates GSK3ß, an enzyme that tags other proteins with phosphate. In nerve cells dedicated to pain relay in the spinal cord, GSK3ß tags d-catenin
(d-CAT), which routs d-CAT to the cellular garbage bin. Without d- CAT in the cells’ nucleus, the Kcc2 gene remains switched off. This in turn makes the pain relay neurons run full of chloride which makes them electrically more jittery, with chronic “refractory” pain a result.
Right-hand panel Treatment with Kenpaullone inhibits GSK3b’s phosphate-tagging capability, so that d-CAT becomes untagged, which clears the way to the nerve cells’ nucleus. There it binds to the DNA region of the Kcc2 gene critical for switch-on or switch-off, the promoter. By binding there, d- CAT reverts the switch-off to switch-on and the Kcc2 gene is running again, making KCC2 protein. KCC2 in turn pumps chloride ions out of the pain-relay nerve cells, making them electrically more stable. This leads to circuit repair and pain relief, based on resetting of the genetic switches. Instead of Kenpaullone, d-CAT can serve as payload of a gene therapy approach that directs expression of d-CAT and hence KCC2 to pain relay nerve cells in the spinal cord.

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Webinar – Dr Jeremy Russell

Trigeminal Neuralgia Association Australia are delighted to provide our link to the webinar presented by Dr Jeremy Russell in Dec 2022.

This webinar completes our program for 2022

Dr Jeremy Russell is one off our distinguished Medical Board Advisors, and has generously provided his time and expertise to assist all sufferers of trigeminal neuralgia.


 TNAA Webinar – Dr Jeremy Russell Trigeminal Neuralgia Treatment Options – YouTube

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5.2 Acupuncture

FACIAL PAIN: A 21st CENTURY GUIDE For People with Trigeminal Neuralgia Neuropathic Pain 5.2 Acupuncture Gary Stanton, MD Acupuncture is an option in the treatment of TN. Acupuncture was developed in China 2,500 to 3,000 years ago, or perhaps even earlier than that. Traditional acupuncture was conceptualized in traditional Chinese terms, with constructs such as […]
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Neuromodulation – for Trigeminal Neuralgia

Our Vice President and Tasmania support group leader, Helen Tyzack, updated her group about neuromodulation for trigeminal neuralgia back in 2021.  She has provided the information she gathered, and we hope it may provide education and understanding about this treatment

Neuromodulation. In italics below I have added the contents of emails I previously sent to all those on my database. The first email was dated 22nd May 2021.

Yesterday it was exciting to watch and listen to the Webinar from the USA at 9am; chaired by the president of the Facial Pain Association of America Dr Jeffrey Brown interviewing a Member of their Medical Board, Dr Konstantin, (an expert in neuromodulation of facial pain).  Previously, thanks to member Peter, I had sent you the information for you to link in. I received an immediate response yesterday from Peter after the Webinar and I wonder how many others took up this excellent opportunity.

 This free opportunity was excellent but whether it was useful depends on your circumstances.  So, what did I learn?   In brief,

  • Neuromodulation is management, not cure, by a non-destructive change in our nerve activity – using a device
  • The device delivers non-painful sensations to the nerve.
  • Neuromodulation is minimally invasive
  • Neuromodulation can be facilitated inside our body or outside depending on need and circumstances.
  • Neuromodulation always involves the use of small devices. That is, the chemical modulation of our nerves by our medications does not count as neuromodulation.
  • Neuromodulation does NOT work for people with Typical Trigeminal Neuralgia and usually makes the pain worse.
  • Neuromodulation does work for people with neuropathic pain on the trigeminal nerve; it is most effective for those who have more or less constant continuing unpleasant pain. Some sufferers with Typical TN can, over time, develop this neuropathic continuous facial pain – either with or without the Typical TN (and its sharp shooting electric shocks).  The neuromodulation may (and may not) work for such people.
  • The process is for the specialist to test a potential patient with an external device over a week to 10 days making adjustments so that the sufferer can work out whether this neuromodulation process might be comfortable for them and reduce or remove the pain.  If all works well then, a device is implanted – and can be there for up to 15-18 years if need be.  If there a period of 6 months without the pain, the thinking is that the device can be removed, and neuromodulation is no longer required.
  • Usually, you do NOT get the ideal result first up and it needs reworking so should be seen as a work in progress.  Every person’s body is unique and therefore the device controls have to be uniquely set up.
  • Once a week the device needs to be recharged and this takes about 30-40 minutes
  • Neuromodulation also works well with sufferers of Occipital Neuralgia at the back of the head but does not work for migraines.
  • Who does neuromodulation treatments?  Find only the most experienced. Beware of someone who says they have 100% success – they may have only treated one or two people. The safest practitioner is the one who has already encountered complications with this process and has safely managed and solved the problems; the more complications (not of their own doing) they have safely coped with the better.
  • How long before you feel relief after the device is implanted? Rarely immediately and mostly hours, days or weeks later.  The message was to be open minded and not to panic if the response is not fast.  Allow time for your body to adjust

Main point:  Not every treatment will work for every person. No treatment will work all the time.

 I am fortunate at the moment not to be taking medications or in pain.  But I am mindful that the time will come when the pain returns. This Webinar was helpful because I now know more about my options for managing the pain.  In Tasmania where would I go for advice? I would be talking with members of the Trigeminal Neuralgia Associations of Australia’s Medical Advisory Board.

My second email was dated 10th August.

A few months ago, I told you I had listened to/watched webinars on the topic of Neuromodulation as a treatment for Trigeminal Neuralgia pain. Afterwards, I set out to determine if a specialist might come to Tasmania and talk to people in our Support Group and any others who might be interested.

Since then, I have been exchanging emails with Dr Nick Christelis, the President of the Neuromodulation Society of Australia and New Zealand. Recently, we talked by phone about the options, but a visit to Tasmania by a specialist to meet with TN sufferers is not on the cards.  However – 

Firstly:

Nick confirmed there was not a specialist in Tasmania, but he explained that he had used neuromodulation on patients with Trigeminal Neuralgia. He would welcome contact from any Tasmanian sufferers and be prepared to do an initial Telehealth consultation. His contact details are on the website: https://painspecialistsaustralia.com.au and his consultation and surgical location is within Warringal Private Hospital in the Melbourne suburb of Heidelberg, Victoria. Phone 1300 798 682.  If you read through this page and watch the video, then you will understand more about the services he offers.  His site has this to say about Nick:

Nick now practices 100% within the field of pain medicine. He is an interventional pain specialist combining a multidisciplinary team approach with advanced pain interventional techniques like nerve and joint blocks, epidural injections, radiofrequency ablation, pulsed radiofrequency, spinal cord stimulation and other advanced neuromodulation techniques.

Secondly:

Nick explained that a quarterly webinar is offered from within his organisation and can be accessed on the bellow link

Events | Ramsay Health Care

Please note that I have no experience of neuromodulation and no experience of Nick’s capabilities, so this email is not meant to be a recommendation. Rather, I am letting you know about this option, in case neuromodulation is a process which could improve your quality of life. 

If you decide to try this, I would be very interested to know what the process is and all the ins and outs. Not to mention whether it was useful for you and reduced, removed your pain. I am sure other sufferers would also be interested so please keep me posted. 

For facial pain sufferers in other mainland states, I recommend you read through the Neuromodulation Society of Australia and New Zealand website to find specialists close to you.

Extra Q&A after the recent webinar on neuromodulation pain management produced by the USA Facial Pain Association

1. Can a TENS unit applied somewhere help? Is the concept of neuromodulation similar to using a TENS unit? thank you.

The TENS is indeed one of the types of neuromodulation, and we do recommend trying it in patients who can tolerate placement electrodes onto painful regions. It tends to be much less effective than other neuromodulation approaches, but is definitely worth trying due to its low invasiveness. Keep in mind, that pain that does not respond to TENS may still be relieved by invasive neuromodulation with implanted devices.

2. Explain the relationship between neuromodulation and neuroplasticity?

Neuromodulation in many ways relies on neuroplasticity – we are trying to modify neural activity by adding neuromodulation signals, and neural plasticity plays a major role in cooling down hyperactive parts of the nervous system that are responsible for development of pain in the first place.

3. “Explain foramen ovale stimulation?” What’s the difference

I am not aware of “foramen ovale stimulation” – most likely, the procedure which is referred here is the stimulation of the trigeminal ganglion (Gasserian ganglion) that is reached through foramen ovale. This approach is known for many years but is rarely used, mostly because it is difficult to keep electrodes in that location as they tend to migrate over time. In principle, however, the trigeminal ganglion stimulation is a very effective approach to control neuropathic facial pain and may be considered if the pain involves several trigeminal branches at once.

4. Can it be used for a patient with a pacemaker?

Yes, neuromodulation can be used in presence of pacemakers and defibrillators. Your doctors need to be aware of these devices so the proper precautions may be made in choosing the device and its location in the body.

5. What is the success related to pain as a result of acoustic neuroma surgery/radiosurgery?

The mere presence of acoustic neuromas, the surgery to remove the tumor, and sometimes radiosurgery for the tumor may result in development of facial pain. Sometimes it presents as secondary trigeminal neuralgia and its treatment resembles trigeminal neuralgia management algorithm, but in some cases the patients develop trigeminal neuropathic pain or occipital neuralgia, and these conditions may great indications for neuromodulation.

6. Would it help with Geniculate Neuralgia?

The pain of geniculate neuralgia has not been investigated as an indication for neuromodulation, or at least I have not heard of it. The classical geniculate neuralgia may require either microvascular decompression or, more often, an open rhizotomy of nervus intermedius – this is what I normally recommend to my patients.

7. Once implanted, can the patient stop taking medications?

Yes, it is possible – but we usually start considering weaning pain medications only after the patients report symptomatic improvement from neuromodulation. Majority of patients are able to significantly reduce the amount of their pain-relieving medications as a result.

8. How much experience does Dr Slavin has with this? How many has Dr Slavin done?

Neuromodulation is a large part of my practice ever since I completed my fellowship in 1999 – and I do between 100 and 150 neuromodulation surgeries every year. Very few of these surgeries are done for facial pain as most facial pain patients I see end up having other interventions, including microvascular decompressions, percutaneous rhizotomy, radiosurgery, etc. Most neuromodulation surgeries in my practice are still done for pain in lower back and extremities, Parkinson disease and tremor, epilepsy and other functional neurosurgical conditions.

9. If I had an MVD without any pain relief, would this help?

Neuromodulation is generally recommended for trigeminal neuropathic pain and not for trigeminal neuralgia. If the patient’s typical trigeminal neuralgia did not improve with microvascular decompression, we would usually consider either repeating the decompression or proceeding with percutaneous interventions. If the pain is non-neuralgic but rather neuropathic in nature, neuromodulation would be an appropriate thing to consider.

10. Are the electrodes ever implanted into the brain and if so, where?

The brain stimulation for facial pain is usually reserved for patients with anesthesia dolorosa – the electrodes are placed either over the surface of the brain (so called motor cortex stimulation) or in the depth of the brain in the area of thalamus or brainstem (so called deep brain stimulation).

11. I am just finishing TMS therapy. It has not helped me. I like Dr. Brown’s suggestion to “adjust the magnet.” How can the Dr. find the correct “spot” for neuropathic pain?

It may be challenging to find the right spot for TMS. We usually recommend finding the face representation in the contralateral motor cortex or focusing stimulation at pre-motor area (which is used for treatment of depression).

12. Following left craniotomy for Trigeminal Schwannoma I have a mix of numbness on lower jaw but extremely sensitive and continuous pain on temple, cheek, and upper jaw. Is the neuro modulation compatible when both numbness and sensitivity are combined?

To answer your question, it would be important to find out whether the numbness is complete or partial. Stimulation of peripheral branches may help in case of partial numbness. Complete numbness may necessitate stimulation of the uppermost cervical spinal cord, the deep brain structures or the motor cortex.

13. Hi, I have a question from the webinar. Dr. Slavin described neuromodulation, if I understood correctly, as an option for trigeminal neuropathic pain but not trigeminal neuralgia and described TN2 symptoms as neuropathic pain. Just to clarify before I get my hopes up, is “trigeminal neuropathy” the same thing as TN2?

Trigeminal neuropathic pain is different from TN2 but there is certain overlap between them. As a matter of fact, about 20 years ago we published a theory that postulated a possible transition from TN2 to trigeminal neuropathic pain as a part natural history of this condition. Right now, we do not recommend neuromodulation for TN2, but use it routinely and frequently for trigeminal neuropathic pain.

The original webinar published by the FPA can be watched below –


Facial Pain Association Neuromodulation – YouTube

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MLS Treatment Therapy

So what is MLS Treatment Therapy, and how can it help sufferers of trigeminal neuralgia?

What is a Multi Wave Locked System?

The Multiwave Locked System (MLSÂŽ) is a new patented LLLT system that combines 905nm pulsed emissions with 808nm continuous emissions.I

It was developed by ASA Laser to help overcome some of the limitations on previous LLLT systems. The aim is to produce simultaneous actions on pain, inflammation and oedema. With the MLSŽ system it is possible to achieve strong anti-inflammatory, anti-oedema and analgesic effects simultaneously and in a short period of time.

The unique synchronised laser beam delivers a balance of the two wavelengths and powers providing safe and effective delivery. The optical design of the delivery system transfers energy up to 3 – 4 cm deep to effect tissue at a cellular level. The synchronised wave results in a synergistic effect where both the analgesic and anti-oedema effects are greater than if two single lasers had been used.

Research suggests for lasting effects from MLS Laser you will likely require 5-6 treatments depending on how your condition responds. Often you will experience a noticeable improvement after just 2 treatments.

For further information about the technology please See Here

This technology has been utilised for a number of years and research has been undertaken  Successful treatment for neuropathic pain with MLSŽ: a case study.

Some clinics use different terminology, however the MLS is used to deliver the treatment.

How does it work?

MLS Laser Therapy is a medical breakthrough therapeutic device with unparalleled applications and treatment outcomes. The laser works by converting light into biochemical energy, resulting in normal cell function, which causes symptoms (PAIN) to reduce significantly.

The primary biological action of PBM (MLS) Therapy results from stimulation of cellular transport mechanisms in the mitochondria, cell membranes and epithelial tissues. This action causes the release of vasodilating chemicals, the stimulation of DNA and RNA (building blocks) synthesis, an increase in enzyme production, normalisation of tissue Ph and increased ATP production (healing of the cells from the inside).

 

10 BENEFITS OF MLS LASER THERAPY

  1. Anti-inflammatory: MLS Laser Therapy has anti-oedema effect as it causes vasodilation, but also because it activates the lymphatic drainage system which drains swollen areas. As a result, there is reduction in swelling caused by bruising or inflammation.
  2. Analgesic: MLS Laser Therapy has a beneficial effect on nerve cells, it blocks pain transmitted by these cells to the brain which decreases nerve sensitivity.  Also, due to the decreased inflammation, there is less oedema and less pain.  Another pain blocking mechanism involves the production of high levels of pain killing chemicals such as endorphins and enkephalin from the brain and adrenal gland.
  3. Accelerated Tissue Repair and Cell Growth: Photons of light from the laser penetrate deeply into tissue and accelerate cellular reproduction and growth.  The laser light increases the energy available to the cell so the cell can take on nutrients faster and get rid of waste products.  As a result of exposure to laser light, cells are repaired faster.
  4. Improved Vascular Activity: Laser light will significantly increase the formation on new capillaries in damages tissue which speeds up the healing process, closes wounds quickly and reduces scar tissue.  Additional benefits include acceleration of angiogenesis, which causes temporary vasodilation and increase in the diameter of blood vessels.
  5. Increases Metabolic Activity: MSL Laser Therapy creates higher outputs of specific enzymes, greater oxygen and food particles loads for blood cells.
  6. Trigger Points and Acupuncture Points: MLS Laser Therapy stimulates muscle trigger points and acupuncture points on a non-invasive basis providing musculoskeletal pain relief.
  7. Reduced Fibrous Tissue Formation: MLS Laser Therapy reduces the formation of scar tissue following tissue damage from cuts, scratches, burns or surgery.
  8. Improved Nerve Function: Slow recovery of nerve functions in damaged tissue can result in numbness and impaired limbs.  Laser light speeds the process of nerve cell reconnection and increase the amplitude of action potentials to optimise muscle healing.
  9. Immuno-regulation:Laser Light has a direct effect on immunity status by stimulating immunoglobulins and lymphocytes.  Laser emissions are absorbed by chromophores (molecule enzymes) that react to laser light.  Upon exposure to the laser, the enzyme flavomononucleotide is activated and starts the production of ATP (adenosine-triphosphate), which is the major carrier of cell energy and the energy source for all chemicals reactions in the cells.
  10. Faster Wound Healing: Laser light stimulates fibroblast development in damaged tissue. Fibroblasts are the building blocks of collagen, which is the essential protein required to replace old tissue or to repair tissue injuries.  As a result, Laser Therapy is effective post surgically and in the treatment of open wounds and burns.

An interesting  in depth article covering every thing you need to know about MLS laser treatment in America, the history, the believers, the skeptics, the medical profession, the politicians and the people who use it

 Does it really work – blog

Pain clinics around Australia are now using this technology see below for examples – please note we do not recommend providers and suggest you discuss any new treatment options with your medical practitioners.

Introducing MLS Laser Therapy The first of its kind on the Central Coast

 

MLS Laser Therapy

Latest Technology

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4 What to Do When Your Surgeon Says There is Nothing Left to Do

FACIAL PAIN: A 21st CENTURY GUIDE 4 What to Do When Your Surgeon Says There is Nothing Left to Do For People with Trigeminal Neuralgia Neuropathic Pain By Jeffrey A. Brown, MD (USA) You think you will have a microvascular decompression (MVD), but there is no compression. Your pain returned after your MVD, and your doctor […]
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Tasmania Support Group Meeting with Mr Jeremy Russell

In March of this year, Helen Tyzack our Tasmanian Support Group Leader arranged an informal zoom webinar, presented by Mr Jeremy Russell

Mr Jeremy Russell is an Australian trained neurosurgeon who manages all general neurosurgical conditions. He has subspecialty expertise in both cerebrovascular and skull base neurosurgery, having obtained fellowships in both areas at the Toronto Western Hospital in Canada. He uses state of the art intraoperative technology to perform angiograms (vessel imaging) and neuromonitoring when appropriate, significantly reducing the potential risk of stroke to patients.

Jeremy is a member of our Medical Advisory Board and is always happy to assist our members with advice and time which we really appreciate

We have been provided with the power point presentation Trigeminal Neuralgia - Mr Jeremy Russell and the recording of the meeting below.  We hope you find both useful

 

 

 

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3.6 CyberKnife: Should I Be Treated by It?

FACIAL PAIN: A 21st CENTURY GUIDE For People with Trigeminal Neuralgia Neuropathic Pain 3.6 CyberKnife: Should I Be Treated by It? Dr. Jeffrey A. Brown, Neurosurgeon A CyberKnifeÂŽ is a registered trademark term, like Xerox or Coca-Cola, to describe a device that has nothing to do with cyberspace or sharp blades. CyberKnife describes a robot, […]
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